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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD

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Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)


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Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)



Regulation of Stroke Volume

Ventricular stroke volume (SV) is the difference between the ventricular end-diastolic volume (EDV) and the end-systolic volume (ESV). The EDV is the filled volume of the ventricle prior to contraction and the ESV is the residual volume of blood remaining in the ventricle after ejection. In a typical heart, the EDV is about 120 ml of blood and the ESV about 50 ml of blood. The difference in these two volumes, 70 ml, represents the SV. Therefore, any factor that alters either the EDV or the ESV will change SV.

SV = EDV - ESV

For example, an increase in EDV increases SV, whereas an increase in ESV decreases SV.

There are three primary mechanisms that regulate EDV and ESV, and therefore SV.

Preload

stroke volume regulation
Changes in preload affect the SV through the Frank-Starling mechanism. Briefly, an increase in venous return to the heart increases the filled volume (EDV) of the ventricle, which stretches the muscle fibers thereby increasing their preload. This leads to an increase in the force of ventricular contraction and enables the heart to eject the additional blood that was returned to it. Therefore, an increase in EDV results in an increase in SV. Conversely, a decrease in venous return and EDV leads to a decrease in SV by this mechanism.

Afterload

Afterload is related to the pressure that the ventricle must generate in order to eject blood into the aorta. Changes in afterload affect the ability of the ventricle to eject blood and thereby alter ESV and SV. For example, an increase in afterload (e.g., increased aortic pressure) decreases SV, and causes ESV to increase. Conversely, a decrease in afterload augments SV and decreases ESV.  It is important to note, however, that the SV in a normal, non-diseased ventricle is not strongly influenced by afterload. In contrast, the SV of hearts that are failing are very sensitive to changes in afterload.

Inotropy

Changes in ventricular inotropy (contractility) alter the rate of ventricular pressure development, thereby affecting ESV and SV. For example, an increase in inotropy (e.g., produced by sympathetic activation of the heart) increases SV and decreases ESV. Conversely, a decrease in inotropy (e.g., heart failure) reduces SV and increases ESV.

It is important to note that the effects of changes in EDV and ESV on SV are not independent.  For example, an increase in ESV usually results in a compensatory increase in EDV.  Furthermore, if SV is increased by increasing EDV, this can lead to a small increase in ESV because of the influence of increased afterload on ESV caused by an increase in aortic pressure.  Therefore, while the primary effect of a change in preload, afterload or inotropy may be on either EDV or ESV, secondary changes can occur that can partially compensate for the initial change in SV.  For a more detailed description of these interactions, see the web pages describing preload, afterload, or inotropy.

Revised 04/02/07



DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.